How Do Different Patterns Of Injury Influence Psychiatric Disorders?

There is a lack of research on the impact of various injuries on mental illnesses. In a majority of cases, localized and diffuse lesions typically coexist in traumatic brain injury.

The following conditions may exacerbate delirium: infections, pharmaceuticals (barbiturates, opiates, steroids), withdrawal from drugs or alcohol, seizures, brain hypoxia, structural damage, infections, and electrolyte imbalance.

After a TBI, delirium may occur in the patient even in the absence of any past medical history. In such a case, the physicians inquire about past drug and alcohol usage because the patient may be abruptly halted owing to an accident that causes delirium. Prominent risk factors: advanced age, concomitant serious illnesses, polypharmacy, basal ganglia, and lesions in the right hemisphere.

Agitation

Patients with agitation typically stay in hospitals for longer periods of time because their injuries are more severe and cause them to miss more time from treatment. Agitation is a common and serious issue in acute rehabilitation settings. It affects one-third to one-half of patients in rehabilitation settings. It is particularly noticeable in patients who have damage to their frontal lobes.

Post-Traumatic Epilepsy (pte)

PTE is caused by cerebral scars and residual foreign bodies that frequently form epileptic foci. Penetrating injuries are associated with a higher risk of PTE than blunt or blast injuries. Patients who abuse alcohol are also at a higher risk of developing PTE. Only seizures that occur or reoccur after seven days following a traumatic brain injury (TBI) are classified as PTE. Anti-epileptic drugs (AEDs), such as phenytoin or levetiracetam, are frequently used as prophylaxis following a severe traumatic brain injury (TBI) to reduce early post-traumatic seizures. There is no evidence that AEDs can lower the prevalence of PTE, which occurs after 7 days of injury

PTE accounts for 5–6% of all epileptic cases. Injury complicated partial seizures, which are followed by secondary generalization, are the typical focal point of PTE. Using AEDs prophylactically for the first seven days following a traumatic brain injury lowers the chance of seizures during this period. Extended use of AEDs or mild to severe traumatic brain injury has little impact on post-traumatic epilepsy

AEDs are well known for their severe adverse effects and for preventing the neuroplasticity that is necessary for healing. For severe TBI patients, an AED should not be used more than seven days after the accident. AED prophylaxis should also be totally avoided in patients with mild to moderate traumatic brain injury. Research has indicated that in individuals with mild traumatic brain injury, PTE promotes psychogenic non-epileptic seizures.

Most patients with moderate traumatic brain injury (TBI) experience convulsion disorders, faux seizures, or psychogenic non-epileptic seizures, which may or may not be actual seizures.

Post-Concussion Syndrome

Headache is dull, nonspecific, and unending; it can get worse with movement, bending, work, or alcohol use. Symptoms include headache, memory impairment, and sleeplessness. Most common aftereffects of mild head trauma, with one or more of the core symptoms lasting for two to three months. Chronic headaches are a side effect of prolonged analgesic usage, though. NSAIDs and TCAs can be used to relieve headaches. Antimigraine can also be used to relieve headaches with a moderate brain injury.

Mild amnesia, inattention, distractibility, and slower information processing are symptoms of memory impairment. Additional symptoms include anxiety, mood swings, photophobia (inability to endure light), phonophobia (inability to handle loud noises), and dizziness.

Clinical Features Of Early Recovery Phase

Neurobiological Changes In Tbi

Experiments have demonstrated that TBI causes both necrotic and apoptotic cascades to cause cell death. It has also been shown that TBI causes diffuse neuronal damage and cell loss in specific vulnerable regions of the prefrontal cortex, hypothalamus, striatum, amygdala, and forebrain nuclei. Finally, delayed post-TBI processes include microglial activation and the release of inflammatory cytokines.

Long-lasting alterations in neuronal degeneration and neuronal circuitry are produced by a complex interplay between delayed post-TBI events and repair and regeneration processes. Reactive synaptogenesis and axonal sprouting are involved in repair and regeneration processes.

Post-Traumatic Changes In The Neurotransmitter (NT Systems

Three important NT systems associated with TBI – glutamate, cholinergic system, and ascending biogenic amine pathways

Glutamate

Excitotoxic neuronal injury is primarily caused by an excitatory NT. The mechanism of excitotoxic injury starts when sodium and chloride ions enter the neurons, causing cytotoxic edema. This causes an influx of calcium ions, which in turn causes an increase in the expression of transcription factors, acute phase proteins, caspases, and proteolytic enzymes, which in turn causes neuronal apoptosis. Patients with traumatic brain injury (TBI) have higher glutamate concentrations in their CSF for several days. Based on preliminary data, glutamate antagonists like ketamine and glutamate release inhibitors like riluzole may be used to treat TBI patients.  

Also Read: Traumatic Brain Injury- Epidemiology And Pathology

Cholinergic System

The cholinergic system is affected by a traumatic brain injury (TBI) in two ways: immediately after the injury, cholinergic activity increases, and blocking the increase in acetylcholine caused by excitation of basal forebrain nuclei at the time of injury may prevent behavioral deficits and the loss of neurons.

Hypofunction of the cholinergic state may occur, but the precise implications are uncertain; • Later effects in the post-TBI course; • Cholinesterase inhibitors appear to improve cognition in TBI in a manner similar to that seen in dementia cases; preliminary clinical data.

Ascending Biogenic Amine Pathways

The severity of a traumatic brain injury as determined by the GCS score is correlated with fluctuating levels of catecholamines. A sustained increase in synaptic NTs leads to the subacute or chronic down-regulation of aminergic transmission, which ultimately results in depressive symptoms.

It influences both the initial course of treatment and the long-term results of traumatic brain injury.  Mania and hypomania symptoms are caused by dysregulation of the mesolimbic and mesocortical dopamine pathways as a result of prefrontal injury.

Hope you found this blog helpful for your Psychiatry residency Neurology and General Medicine preparation. For more informative and interesting posts like these, keep reading PrepLadder’s blogs.